POTENTIAL POSTERIOR SEGMENT COMPLICATIONS OF INTRAVENOUS DRUG ABUSE
AMANDA S LEGGE, B.S.
ABSTRACT
CASE REPORT: Two patients present with similar chief complaints: a sudden, painless, decrease in vision that has remained
stable for the past few days. Upon dilation, retinal and choroidal infiltrates led to additional questioning regarding social
history. Both patients then admitted to intravenous drug abuse for the past 10+ years. The urgency of the situation was
stressed and both were referred to a local hospital for cultures and intravenous/intravitreal antimicrobial therapy as
indicated.
DISCUSSION: Intravenous drug abuse is associated with a remarkable amount of local and systemic complications. Numerous
ophthalmological consequences can be observed with or without patient symptoms. Observation of suspicious signs warrants
a thorough history including recreational drug use. Eliciting a connection between intravenous drug abuse and clinical signs is
important in order to quickly and accurately diagnose and manage both the ocular and systemic complications associated.
Injection of intravenous drugs is directly
associated with a variety of local and systemic
complications. It can have detrimental effects
on ocular tissue. The most devastating visual
signs include choroidal and retinal nodules,
infarction, and inflammation. This is especially
true because these lesions typically occur in the
posterior pole near the macula.
Eliciting a thorough history is crucial for
appropriate tests, cultures, and treatment.
Prompt diagnosis and management is of utmost
importance to decrease both ocular and
systemic morbidity and mortality.
The following case reports illustrate infections
and possible posterior segment consequences
secondary to intravenous drug abuse and the
management of such.
CASE REPORT 1
HISTORY
The patient is a 30-year-old white male who
presented to our office for the first time with a
chief complaint of decreased vision O.S. greater
than O.D. The vision decreased suddenly
approximately two weeks ago and has remained
stable O.U. He denied floaters or photopsia,
diplopia, pain, or discomfort.
The patient’s medical history is remarkable for
posttraumatic stress disorder, bipolar affective
disorder, chronic cluster headaches, and
depression. He does not take any medications.
The patient’s ocular history is unremarkable as
he reports never having a formal eye exam.
Family ocular and medical history is
unremarkable.
Prior to vision loss the patient experienced lowgrade fevers, severe cluster headaches, and
diffuse joint pain for one month. An extensive
lab work-up was performed by his primary care
physician (PCP) and all results were within
normal limits including CBC, PT/PTT, INR, lupus
anticoagulant, amylase, lipase, FTA, rheumatoid
factor, ANA, RPR, urinalysis, and HIV screening.
He also had a negative CT scan of the head and
chest without contrast. He has not seen his PCP
since receiving these results. He reports that
these symptoms seem to be worsening.
The patient admits to intravenously injecting
crack cocaine dissolved in vinegar. He admits to
using approximately 10 to 15 times per week for
the past five years. He states that he is aware of
the risks of his behavior but has not attended
any counseling or rehabilitation for it.
DIAGNOSTIC DATA
The patient’s unaided visual acuity was 20/40
O.D. and 10/300 O.S. with direct fixation. No
improvement with pinhole. He was 20/200 with
eccentric fixation O.S. Pupils were equal, round,
and reactive to light without an afferent defect.
Extraocular motility testing found no restrictions
of muscle movement. Confrontation visual fields
were full to finger counting O.D., O.S.
Intraocular pressures via applanation were 11
mmHg O.D. and 12 mmHg O.S. Anterior
segment examination was unremarkable. No
inflammatory cells or protein flare was noted in
the anterior chamber.
Gonioscopy O.U. revealed the most posterior
structure in all quadrants to be the ciliary body
face. No sign of microhyphema, microhypopyon,
peripheral
anterior
synechiae,
or
neovascularization O.D., O.S. was noted.
Posterior segment evaluation revealed multiple
choroidal and retinal infarcts of varying duration
and Roth spots throughout the posterior pole
O.U. Nerve fiber layer hemorrhages and
exudates as well as retinal infiltrates were
noted, indicating a septic chorioretinitis. The
optic nerves were flat, pink, and distinct with no
sign of disc edema.
Figure 1. Fundus Photography illustrating bright retinal infiltrates, hemorrhages, dull choroidal infarcts O.U.
and exudates O.D.
Figure 2. Encircled magnified views. Left: Roth spot with obvious infarct surrounded by lighter hemorrhage.
Right: Retinal infiltrate upper left and choroidal infarct lower right of the magnified circle.
Figure 3. Fundus autofluorescence photograph illustrating the multiple hemorrhages surrounding the white infarcts (Roth
spots) blocking the autofluorescence.
The macula O.S. was directly affected,
correlating with his severe decrease in vision in
that eye. The right eye had subtle macular
edema and exudates accounting for his mild
decrease in vision.
Additional blood work was ordered including
repeat CBC with platelet count and differential,
troponin I, Westergren sedimentation rate, Creactive protein, and a blood culture. This was
obtained the same day as presentation.
DIAGNOSIS AND FOLLOW-UP
A diagnosis of septic chorioretinitis was made.
The emergent nature of this condition as well as
the suspected underlying cause of bacterial
endocarditis was strongly stressed to the
patient. An immediate referral was made to a
local hospital indicating the need for a
transesophageal echocardiogram (TEE) to
confirm
the
diagnosis
and
prompt
administration of intravenous antibiotics.
He did not report to the hospital as
recommended. Upon investigation a relative
informed us that he had died from a gunshot
wound to the head. Apparently he was
murdered the night of the referral. This was
confirmed.
The lab results revealed an elevated troponin I,
sed rate, and CRP. CBC was still within normal
limits. Blood culture revealed growth of
staphylococcus aureus, possibly methicillin
resistant.
Although a TEE could not be obtained to
confirm, a presumed diagnosis of bacterial
endocarditis caused by S. aureus was made.
CASE REPORT 2
HISTORY
The patient is a 42-year-old white female. She
presented to the office with a chief complaint of
severe blurred vision O.D. for the past week.
The vision decreased rapidly and painlessly over
the course of two to four days and has remained
stable since that time. No complaint of pain,
irritation, diplopia, photopsia, or floaters was
elicited. She did not have any associated signs or
symptoms.
The patient’s medical history is unremarkable,
but she admitted she has not seen a physician in
at least 10 years. Her ocular history is
unremarkable. She does wear glasses since the
age of 12. Her current prescription is at least 4
to 5 years old. Family ocular and medical history
was unremarkable.
The patient is an admitted intravenous heroin
user since the age of 15. In the past year she has
cut back to using only a few times per month.
She admitted to using up to six times daily in the
past. She stated that she is aware of the risks of
her behavior. She has tried multiple counseling
sessions over the last 5 years. She has never
enrolled in a formal rehabilitation program.
DIAGNOSTIC DATA
Upon evaluation the patient’s aided visual acuity
was 20/100 O.D. without pinhole improvement
and 20/20 O.S. Pupils were equal, round, and
reactive to light without an afferent defect.
Extraocular motility testing found no restrictions
of muscle movement. Confrontation visual fields
were full to finger counting O.D., O.S.
Color vision was 14/14 O.D., O.S. and no red
desaturation was noted.
Intraocular pressures via applanation were 18
mmHg O.D. and 19 mmHg O.S. Anterior
segment examination was unremarkable. No
inflammatory cells or protein flare was noted in
the anterior chamber.
Gonioscopy O.U. revealed the most posterior
structure in all quadrants to be the ciliary body
face. No sign of microhyphema, microhypopyon,
peripheral
anterior
synechiae,
or
neovascularization O.D., O.S. was noted.
Posterior segment evaluation revealed a round,
yellow-white pre-retinal lesion with surrounding
telangiectasia O.D. and 2+ posterior vitreal cells.
Trace to 1+ cells were noted in the anterior
vitreous.
and vitreal inflammation than true disc edema
as no afferent defect was noted on pupil testing
and color vision was normal.
The
left
fundus
was
unremarkable.
The optic nerve O.D. had blurred margins;
however this was likely secondary to traction
Figure 4. Color fundus photography illustrating the position of the retinal lesion as well as the blurred disc
margins. Few retinal striae can be seen temporal to the lesion.
Figure 5. Magnified red-free image of the retinal lesion illustrating the surrounding telangectatic vessels.
DIAGNOSIS AND FOLLOW-UP
The patient was immediately directed to the
hospital for cultures and intravenous
antimicrobial therapy. The patient underwent
MRI of brain and orbits with and without
contrast, FTA, RPR, HIV screening, Lyme titre,
ACE, toxocara IgG, PPD, chest XRay and CBC
testing as well as blood cultures.
A vitreal culture was taken the following day. A
mold infection of unknown species was
identified in the vitreal cultures. All other testing
was negative. The patient was started on
amphotericin B intravenously as this is broad
spectrum and the exact species could not be
identified. The mold has not been reproducing
in the mycology lab. This is necessary for species
identification.
Because amphotericin B has poor vitreal
penetration when prescribed orally the patient
was also started on 5µg / 0.1 mL intravitreal
injection of amphotericin B. She has had 2
intravitreal injections in 5 weeks.
The patient was hospitalized for 5 weeks and
was released. The patient has transferred from
intravenous to oral amphotericin B as managed
by her infectious disease specialist. The patient
now reports a moderate improvement in vision
with mild distortion. Visual acuities were
measured to be 20/50 O.D. and 20/20 O.S.
Vitreal cells were not observed on this exam.
The pre-retinal nodule has now formed a
fibrotic scar causing retinal traction and retinal
striae. Blood cultures were performed again 2
and 4 weeks after hospital admittance and are
still negative. Eight weeks after culture the mold
was identified as Malbranchea spp.
The patient will be monitored closely for
advancing retinal traction and potential for a
detachment. She has been well educated on the
risks associated with intravenous drug abuse
and will begin rehabilitation next week.
Figure 6. Fundus photography at 5 weeks after original diagnosis and initiation of treatment. Fibrotic scarring
Is now in place of the nodule with moderate traction and retinal striae through the macula and superior vascular arcade.
DISCUSSION
Recreational injection of drugs is directly
associated with a variety of local and systemic
complications. It is also linked to the
transmission of infectious diseases through
needle sharing and sexual activity. The most
serious ocular complications have been
reported from the use of crack or crack-cocaine,
methylenedioxymethamphetamine (MDMA), or
diamorphine (heroin) injections1.
Ophthalmological complications include corneal
ulcers, reduced corneal sensitivity, microtalc
retinopathy, retinal or choroidal infarcts, central
retinal artery or vein occlusion, endophthalmitis,
nystagmus, and cerebrovascular accidents that
cause neuro-ophthalmic manifestations2.
Retinal or choroidal infarct, inflammation, or
infiltrate cause some of the most devastating
visual sequelae as they are typically located in
the posterior pole1. These signs are indicative of
general
septic
chorioretinopathy.
The
underlying cause is bacterial or fungal and less
commonly parasitic. Inflammatory causes of
chorioretinopathy must also be ruled out.
Eliciting a history of illicit intravenous drug
abuse
is
imperative
when
septic
chorioretinopathy is suspected. This aids in
prompt testing for the most common pathogens
associated with this risky behavior and early
initiation of appropriate treatment.
The most common pathogen affecting IV drug
users is bacterial, specifically Staphylococcus,
with the most concerning species being
methicillin resistant S. aureus. Other common
pathogens include streptococci species, gram
negative
bacilli,
enterococci,
fusarium,
2
aspergillus, and candida .
A
serious
presentation
of
bacterial
chorioretinitis in intravenous drug users is
Roth’s spots and choroidal infarcts secondary to
bacterial endocarditis. Roth spots are white
centered hemorrhages that classically are
indicative of bacteremia and bacterial
endocarditis; however they are also seen in
diseases such as leukemia, pernicious anemia,
sickle cell disease, and connective tissue
disorders3.
In bacterial endocarditis, Roth spots are formed
as a result of thrombocytopenia and a low
grade,
disseminated,
intravascular
4
coagulopathy . The clinically viewed white
centered hemorrhages are most likely caused by
anoxia which causes a sudden increase in
venous pressure. This causes capillary rupture
and extrusion of whole blood. Platelet release
causes the coagulation cascade to initiate,
eventually causing a platelet-fibrin thrombus
surrounded by heme5.
Because of this specific pathology, Roth spots
are now part of the standard used to determine
a diagnosis of bacterial endocarditis6.
According to the Duke Criteria, infective
endocarditis is definitely present under three
conditions: two major clinical criteria are
present, one major and three minor clinical
criteria are present, or if five minor clinical
criteria are present. Major clinical criteria
include persistently positive blood cultures for
organisms that are typical of causing bacterial
endocarditis, vegetations or abscesses in heart
valves present on echocardiogram, evidence of
new echocardial damage, or culture evidence of
infection with Coxiella burnetii. Minor critical
criteria include fever, the presence of a
predisposing valvular condition or intravenous
drug abuse, vascular phenomenon (includes
emboli to organs or brain and hemorrhages in
the mucous membranes around the eyes),
immunologic phenomenon (includes Roth’s
spots and Osler’s nodules), and positive blood
cultures that do not meet the strict definitions
of the major criteria7.
Compared to other classification systems, the
Duke Criteria has the highest validity. Multiple
studies have shown its predictive value to be
approximately 80% and it rarely rejects any
infective endocarditis that is ultimately
pathologically confirmed6,7,8. The patient in Case
1, although unable to undergo further testing,
was a probable diagnosis of bacterial
endocarditis according to this criterion. A
definite diagnosis would have required
additional testing including a TEE.
Early treatment of bacterial endocarditis is
crucial to maintaining low morbidity and
mortality rates. Treatment consists of prolonged
parenteral therapy of bacteriocidal agents.
Serial blood cultures are necessary to document
sterilization. In intravenous drug abusers, the
most common pathogen causing bacterial
endocarditis
is
Staphylococcus
aureus,
accounting for over half of these infections9.
The most common treatment regimen for S.
aureus infective endocarditis is intravenous
naficillin and an aminoglycoside for two
weeks10. Several studies have also evaluated a
regimen of oral antimicrobials for intravenous
drug users as many refuse hospitalization. These
have not been as successful. Standard of care
remains a two week hospitalization period with
serial blood cultures11.
Fungal infections can also cause choroidal or
retinal nodules, infarcts, and inflammation in
intravenous drug abusers. However, Roth’s
spots are not typical in fungal or parasitic
infections.
The most common cause of fungal
chorioretinopathy in intravenous drug abusers is
candida12. It often presents as a round, white,
fluffy, lesion with a mild to moderate vitritis.
This must be primarily differentiated from
toxoplasmosis which is similar in appearance;
however the active lesion is often directly
adjacent to a chorioretinal scar. Other
differentials include tuberculosis, syphilis, Lyme
disease, sarcoid, and toxocara3.
Endogenous fungal endophthalmitis is typically
caused first by a chorioretinitis and then
progresses into the vitreous. Transient fungemia
may seed in the highly vascularized choroid13.
Once in the choroid, the yeast proliferates,
invokes an inflammatory response and can
subsequently rupture into the vitreous cavity.
Once in the vitreous cavity the infection is
considered a true fungal endoophthalmitis14.
Treatment consists of oral antifungals, unless
the vitreous is involved. A vitritis in a fungal
infection is best treated with early vitrectomy
and intravitreal Amphotericin B13,15. An
infectious disease specialist should always be
consulted once a diagnosis of fungal
chorioretinitis or endophthalmitis is diagnosed.
The duration of treatment for fungal
endophthalmitis is minimally five weeks and is
ultimately based on improvement of
ophthalmological examinations16.
Unfortunately the species of the mold in Case 2
could not be determined during the treatment
period and therefore broad spectrum antifungals were utilized with moderate success.
Diagnosis of septic chorioretinitis warrants
further investigation into a patient’s social
history, specifically with regards to any
recreational drug use. This is especially true if a
patient is in a high risk population for illicit drug
abuse.
Prompt diagnosis and management is crucial to
lowering the ocular and systemic morbidity and
mortality associated with these findings. Comanaging with an infectious disease specialist
early in the treatment course is advised.
Patient education and rehabilitation services
should be offered and encouraged immediately
following any hospitalization requirements.
REFERENCES
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Firth, A., Ocular Sequelae from the Illicit Use of Class A Drugs, Br Ir Orthopt, 2004; 1: 10-18.
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Later. Annals of Int Med., 1993, Nov; 119(10): 1017-1028.
3
Wills Eye Hospital. The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease.
5th ed. Philadelphia, Pa: Lippincott; 2008.
4
Ling, J., James, B., Classic Signs Revisited: White Centered Retinal Hemorrhages (Roth Spots). Post-grad Med J, 1998;
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Aguilar, G., Blumenkrantz, M, Egbert, P., McCulley, J., Candida endophthalmitis after intravenous drug abuse. Arch
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Omuta, J, et. al., Histopathological Study on Experiemental Endophthalmitis Induced by Bloodstream Infection with Candida
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